No abstract

This study was designed to investigate the cardiovascular effects of sulfur dioxide within the nucleus tractus solitarii. Sulfur dioxide or artificial cerebrospinal fluid was unilaterally applied into the nucleus tractus solitarii of rats, and the effects on blood pressure, heart rate, and arterial baroreflex sensitivity (ABR) were determined. To explore the mechanisms of the effects of intra-nucleus tractus solitarii sulfur dioxide, various inhibitors were applied prior to sulfur dioxide treatment. Unilateral microinjection of sulfur dioxide produced a dose-dependent decrease in blood pressure in anesthetized rats. Significant decreases in heart rate were also seen after unilateral microinjection of 20 and 200 pmol of sulfur dioxide ( P < 0.05). Bilateral microinjection of sulfur dioxide into the nucleus tractus solitarii significantly decreased blood pressure and heart rate and also attenuated ABR. Pretreatment with glibenclamide or nicardipine within the nucleus tractus solitarii did not alter the hypotension or bradycardia ( P > 0.05) induced by intra-nucleus tractus solitarii sulfur dioxide. Pretreatment with 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one, however, significantly attenuated this hypotension and bradycardia. Prior application of kynurenic acid or N (G)-Nitro- l -arginine methyl ester into the nucleus tractus solitarii partially diminished the hypotension and bradycardia induced by intra-nucleus tractus solitarii sulfur dioxide. Our present study shows that sulfur dioxide produces cardiovascular inhibitory effects in the nucleus tractus solitarii, predominantly mediated by glutamate receptors and the nitric oxide/cyclic GMP signal transduction pathway.

Salusin-α and salusin-β are newly found bioactive peptides of 28 and 20 amino acids, respectively, which are widely distributed in the hematopoietic system, endocrine system, and central nervous system. Salusins exert cardiovascular effects, including hypotension and bradycardia; promote vascular inflammation; and so on. However, little information is available yet on the relationships of salusin-β with sepsis. In this study, we investigated the distribution and content of endogenous salusin-β in septic rats. A total of 72 specified pathogen-free (SPF) male Sprague-Dawley (SD) rats were randomly divided into control group (sham operation, n = 36) and experimental group (n = 36) with sepsis rat model by cecal ligation and puncture (CLP). The model group rats were sacrificed after 6, 12, and 24 h of treatment. The concentration of salusin-β in spleen, stomach, small intestine, hypothalamus, and serum specimens was detected by enzyme-linked immunosorbent assay (ELISA). It showed that salusin-β was endogenously generated in rat tissues, including spleen, stomach, small intestine, hypothalamus, and serum. The content of salusin-β in the spleen was higher than that in other tissues. The content of salusin-β in the spleen, stomach, and small intestine, together with the serum level of salusin-β, increased significantly at 6 h after CLP compared with the control group (P < 0.05). The content of salusin-β in spleen and serum peaked at 12 h, and in small intestine, it reached the summit at 24 h. Meanwhile, no significant fluctuations in salusin-β content were observed in the stomach. The content of salusin-β in hypothalamus began to increase at 6 h, and a significant increase appeared 12 h after CLP (P < 0.05). In conclusion, this study shows that the time-dependent alterations of salusin-β in septic rats suggest that salusin-β might be involved in the pathogenesis of sepsis.